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Basics ⬇

Outline

BASICS

Overview!!navigator!!

  • SLD is acute or chronic SL injury of the proximal, body, and/or branches.
  • DSLD is a progressive, debilitating disorder resulting in continuous SL enlargement owing to ineffective collagen fiber repair and generalized interstitial and periligamentous fibrosis.
  • Systems affected—musculoskeletal: palmar/plantar MCIII/MTIII

Signalment!!navigator!!

SLD

  • Performance horses.
  • Hind SLD—Standardbreds, upper level dressage.
  • Thoroughbred racers—SL rupture in catastrophic breakdown

DSLD

Peruvian Paso most common.

Signs!!navigator!!

SLD

  • Acute, insidious, mild to moderate lameness.
  • Lameness resolves with rest; recurs with exercise.
  • ±Forelimb lameness worse on outside of circle.
  • Subtle hindlimb lameness, worse when ridden.
  • ±Localized heat, swelling, pain.
  • ±Palpable thickening, positive limb flexions.
  • ±Fetlock effusion with branch injury.
  • Complete rupture—dropped fetlock, severe lameness

DSLD

  • Acute—stiffness, reluctance to work, back pain.
  • Subtle, chronic intermittent or persistent unilateral to quadrilateral lameness.
  • End-stage—reluctant to move, lie down often.
  • Palpable thickening, pain.
  • Progressive fetlock drop

Causes and Risk Factors!!navigator!!

SLD

  • Foot imbalance, long pasterns, fetlock hyperextension.
  • Back at the knee or tied-in below the knee, straight hock.
  • Axial splint exostosis (“blind splint”)

DSLD

  • Peruvian Paso heritage.
  • Abnormal proteoglycan deposition in connective tissues

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

SLD

  • Proximal front—middle carpal or carpometacarpal joint pain, avulsion/stress MCIII fracture, carpal sheath/retinaculum pain.
  • Proximal hind—tarsometatarsal joint pain, avulsion/stress MTIII fracture

DSLD

Injury-mediated SLD.

Imaging!!navigator!!

US

  • Acute—focal isoechoic/anechoic core lesion.
  • Chronic—decreased echogenicity, abnormal fiber pattern.
  • Increased cross-sectional area.
  • ±Periligamentous thickening, adhesions.
  • Unweighted and “off-incidence” images enhance diagnosis.
  • Dystrophic calcification.
  • DSLD—progressive enlargement, loss of echogenicity and fiber pattern, primarily in branches

MRI

  • Superior to US.
  • SL changes, osseous involvement.
  • Indicated if lameness localized to SL and other imaging normal

Radiography

  • ±Normal.
  • Proximal MCIII/MTIII—subchondral sclerosis, avulsion fracture.
  • Sesamoiditis, sesamoid fracture.
  • Splint bone exostosis or fracture

Nuclear Scintigraphy

SLD often negative; proximal palmar/plantar MCIII/MTIII uptake with bony injury.

Other Diagnostic Procedures!!navigator!!

SLD

  • Diagnostic analgesia—high palmar/plantar, lateral palmar, subtarsal, SL local infiltration.
  • ±Diffusion of intra-articular middle carpal and tarsometatarsal analgesia into proximal SL

DSLD

  • Diagnostic analgesia as for SLD.
  • ±Nuchal ligament biopsy

Pathologic Findings!!navigator!!

DSLD—histopathology: large proteoglycan accumulations in SL(s).

Treatment ⬆ ⬇

TREATMENT

SLD

  • Acute—local and/or systemic analgesics and anti-inflammatory(s).
  • Controlled exercise program—stall rest and hand-walking for weeks to months then gradual return to exercise.
  • Hoof balance, heel support, eggbar shoes.
  • Ancillary therapies:
    • Extracorporeal shockwave therapy.
    • Percutaneous SL splitting (desmoplasty).
    • Palmar/plantar metacarpal/metatarsal fasciotomy.
    • Neurectomy of deep branch of lateral plantar nerve.
    • Intralesional injections (stem cells, platelet-rich plasma, bioscaffold material)

DSLD

  • Local and/or systemic analgesics and anti-inflammatory(s).
  • Controlled exercise program.
  • Stall confinement.
  • Extended heel support, eggbar shoes

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • NSAIDs—phenylbutazone 2.2–4.4 mg/kg SID–BID.
  • Systemic chondroprotective drugs—polysulfated glycosaminoglycan (500 mg IM every 4 days for 7 treatments) or sodium hyaluronate (40 mg IV every 7 days for 3 treatments).
  • Oral glucosamine/chondroitin sulfate powder (1 scoop (3.3 g) BID)

Contraindications/Possible Interactions!!navigator!!

Intralesional corticosteroids.

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • US and lameness every 8–12 weeks.
  • Recurrence of lameness, heat, swelling during rehabilitation prompts stall rest and reexamination

Possible Complications!!navigator!!

Chronic lameness despite treatment.

Expected Course and Prognosis!!navigator!!

  • Convalescence 6–12 months depending on lesion severity.
  • Good athletic prognosis for front proximal SLD; poor for hind proximal SLD.
  • High recurrence in inadequately rested horses.
  • DSLD—poor prognosis

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

SLD

  • MCIII/MTIII avulsion fracture.
  • Splint bone fracture, exostosis.
  • Sesamoid fracture, sesamoiditis

See Also!!navigator!!

Tendonitis

Abbreviations!!navigator!!

  • DSLD = degenerative suspensory ligament disease.
  • MCIII = third metacarpus.
  • MRI = magnetic resonance imaging.
  • MTIII = third metatarsus.
  • SL = suspensory ligament.
  • SLD = suspensory ligament desmitis.
  • US = ultrasonography, ultrasound

Suggested Reading ⬆ ⬇

Dyson SJ. The suspensory apparatus. In: Ross MW, Dyson SJ, eds. Diagnosis and Management of Lameness in the Horse. St. Louis, MO: Saunders, 2003:654–666.

Werpy NM, Denoix JM. Imaging of the equine proximal suspensory ligament. Vet Clin North Am Equine Pract 2012;28(3):507–525.

Author(s) ⬆

Author: JoAnn Slack

Consulting Editor: Elizabeth J. Davidson